Evidence map›Paper›PMID 41383752›Full record

ArticlebioRxiv : the preprint server for biology2025

Metabolic and Redox Pathway Dysregulation in HIV-Associated Coronary Endothelial Dysfunction: Insights into Early-Phase HIV Vascular Dysfunction.

Kshipra S Keole, Syed Bukhari, Anum Minhas, Charles D Cohen, Amelia Wallace, Damani Piggott, Thorsten M Leucker, Kevin Sun, Luigi Adamo, Allison Hays

Abstract readPreprint
In one paragraph

Article in bioRxiv : the preprint server for biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors.

Kshipra S KeoleDivision of Cardiology, Department of Medicine, The Johns Hopkins University School of Medicine, Baltimore, Maryland.ORCID 0009-0001-3867-9501
Syed BukhariDivision of Cardiology, Department of Medicine, The Johns Hopkins University School of Medicine, Baltimore, Maryland.
Anum MinhasDivision of Cardiology, Department of Medicine, The Johns Hopkins University School of Medicine, Baltimore, Maryland.ORCID 0000-0001-6680-0404
Charles D CohenDivision of Cardiology, Department of Medicine, The Johns Hopkins University School of Medicine, Baltimore, Maryland.ORCID 0000-0002-4700-6368
Amelia WallaceDepartment of Epidemiology, Johns Hopkins Bloomberg School of Public Health, Baltimore, Maryland.ORCID 0000-0002-1466-3791
Damani PiggottDepartment of Medicine, Division of Infectious Diseases, The Johns Hopkins University School of Medicine, Baltimore, Maryland.
Thorsten M LeuckerDivision of Cardiology, Department of Medicine, The Johns Hopkins University School of Medicine, Baltimore, Maryland.
Kevin SunDivision of Cardiology, Department of Medicine, The Johns Hopkins University School of Medicine, Baltimore, Maryland.
Luigi AdamoDivision of Cardiology, Department of Medicine, The Johns Hopkins University School of Medicine, Baltimore, Maryland.ORCID 0000-0003-2704-978X
Allison HaysDivision of Cardiology, Department of Medicine, The Johns Hopkins University School of Medicine, Baltimore, Maryland.ORCID 0000-0003-2138-1589

Funding

PATHOPHYSIOLOGY OF MYOCARDIAL DISEASEST32HL007227 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI Chulan Kwon, WENDY S POST · 1985 to 2026
$21.2M
Sex-specific factors, inflammation and vascular health across the lifespan in women living with HIVR35HL172680 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI Allison G Hays · 2024 to 2026
$1.0M
NHLBI NIH HHS R35 HL172680NHLBI NIH HHS T32 HL007227
6 · The paper itself

Abstract

Background: People with HIV (PWH), even with sustained viral suppression on antiretroviral therapy (ART), remain at increased risk for cardiovascular disease. Coronary endothelial dysfunction, a sensitive marker of early vascular injury and a potential target for intervention is common in this population, but its biological basis remains unknown. Methods: We performed a cross-sectional study combining Results: Coronary endothelial dysfunction was more prevalent in PWH with suppressed viral load compared to controls (67% vs 10%, p<0.001). Pathway analysis of differentially expressed proteins between participants with and without endothelial dysfunction highlighted significant dysregulation of glutathione dependent detoxification, oxidative metabolism and fatty acid β-oxidation pathways in individuals with endothelial dysfunction (adjusted p value <0.05). Conclusions: Endothelial dysfunction in PWH on ART is associated with metabolic and redox imbalance. These findings highlight glutathione and fatty acid oxidation related pathways as potential therapeutic targets for reducing cardiovascular risk in this patient population.

Indexed as

coronary endothelial functionmetabolic dysregulationoxidative stressPeople with HIVredox pathway dysregulationSomaScan proteomics

Identifiers

PMID41383752
PMCPMC12694598

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.